Hepatic Macrophages as Targets for the MSC-Based Cell Therapy in Non-Alcoholic Steatohepatitis

Non-alcoholic steatohepatitis (NASH) is a serious public health issue associated with the obesity pandemic. Obesity is the main risk factor for the non-alcoholic fatty liver disease (NAFLD), which progresses to NASH and then to end-stage liver disease. Currently, there are no specific pharmacotherap...

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Bibliographic Details
Published in:Biomedicines 2023-11, Vol.11 (11), p.3056
Main Authors: Kholodenko, Irina V, Yarygin, Konstantin N
Format: Article
Language:English
Subjects:
Animal models
Apoptosis
Autophagy
Blood flow
Cell death
Cell therapy
Clinical trials
DAMPs
Development and progression
Diabetes therapy
Drug approval
Epidemics
Fatty liver
Ferroptosis
Fibrosis
Health aspects
Hepatocytes
Inflammation
Insulin resistance
Kinases
Kupffer cells
Lipid metabolism
Lipids
Liver cancer
Liver cirrhosis
Liver diseases
Macrophages
Mesenchymal stem cells
NAFLD
NASH
Neutrophils
Obesity
Oxidative stress
Pathogenesis
Physiological aspects
Proteins
Public health
Risk factors
Stem cell research
Stem cells
Type 2 diabetes
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Summary:Non-alcoholic steatohepatitis (NASH) is a serious public health issue associated with the obesity pandemic. Obesity is the main risk factor for the non-alcoholic fatty liver disease (NAFLD), which progresses to NASH and then to end-stage liver disease. Currently, there are no specific pharmacotherapies of NAFLD/NASH approved by the FDA or other national regulatory bodies and the treatment includes lifestyle adjustment and medicines for improving lipid metabolism, enhancing sensitivity to insulin, balancing oxidation, and counteracting fibrosis. Accordingly, further basic research and development of new therapeutic approaches are greatly needed. Mesenchymal stem cells (MSCs) and MSC-derived extracellular vesicles prevent induced hepatocyte death in vitro and attenuate NASH symptoms in animal models of the disease. They interact with hepatocytes directly, but also target other liver cells, including Kupffer cells and macrophages recruited from the blood flow. This review provides an update on the pathogenesis of NAFLD/NASH and the key role of macrophages in the development of the disease. We examine in detail the mechanisms of the cross-talk between the MSCs and the macrophages, which are likely to be among the key targets of MSCs and their derivatives in the course of NAFLD/NASH cell therapy.
ISSN:2227-9059
2227-9059
DOI:10.3390/biomedicines11113056